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. 2021 Mar 24;12(4):311. doi: 10.1038/s41419-021-03597-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A IGV tracks showing the chromatin distributions of H3K36M in wild-type (WT), H3.3K36M-, and H3.1K36M-mutant cell lines. B The distribution profiles of normalized H3K36M read density from 5 kb upstream of the TSS to 5 kb downstream of the TES. PRKM reads per kilobase million. C, D Normalized read density of H3K36M from 5 kb upstream of the TSS to 5 kb downstream of the TES in grouped genes with high, medium, and low expression levels. The average read densities of the H3K36M ChIP-seq in H3.3K36M- (C) and H3.1K36M- (D) mutant cells were calculated. The genes were separated into high expression, medium expression, and low expression groups based on their expression levels. E H3K36M enrichment analyzed via ChIP-qPCR. The data are represented by the mean ± SD (N = 3 independent replicates, ***p < 0.001). F Venn diagram illustrating the overlap of the H3K36M peaks in H3.3K36M- and H3.1K36M-mutant cells. The H3K36M peaks in independent H3.3K36M- and H3.1K36M-mutant clones were combined.